分子標的療法薬,イマチニブによる慢性骨髄性白血病の治療(<シリーズ>画期的に進歩した最新の治療法(4))

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Chronic myeloid leukemia (CML) is a poor prognostic disease which is characterized by Philadelphia chromosome: t (9; 22) (q34; q11). The BCR-ABL fusion gene product which is produced by chromosome translocation causes a constitutive active tyrosine kinase, and this enhances proliferation of myeloid hematopoietic lineage cells. Recently, new drug STI571 (Imatinib) which inhibits signal transduction of BCR-ABL fusion gene product has been developed for the treatment of CML. By the use of 400 mg per day, hematological remission was obtained in 96% of newly diagnosed CML patients, major cytological remission in 83%, and complete cytological remission in 68%. For patients at an accelerated phase and at blast crisis, 600 mg per day resulted in hematological remission in 71% and 35%. Major cytological remission was obtained in 28% and 18% respectively, and complete cytological remission in 37% and 14%. Treatment with Imatinib dramatically improved disease-free survival of CML patients in chronic phase, accelerated phase and even at the blast crisis. The use of Imatinib has already become a standard therapy for untreated CML patients. In patients in whom remission was not achieved by Imatinib, co-treatment with interferon or a low-dose cytarabine with Imatinib is suggested. Resistance to Imatinib often develops, and it seems to be a major problem in the clinical use of this medicine.
東京女子医科大学の論文